Cell proliferation and tissue growth are tightly controlled during development. In epithelial tissues in Drosophila melanogaster, these processes are regulated in part by the Sterile-20 kinase Slik (SLK and LOK in mammals) and the tumor suppressor Hippo (Hpo, MST1/2 in mammals). Slik overexpression leads to an increase in tissue size in flies, whereas, slik-/- mutants die before completing development. Overexpressing this protein in the developing wing disc epithelium promotes cell proliferation, consistent with the overgrown wing phenotype in the adults. Moreover, expression of Slik in one population of cells leads to an overproliferation of neighboring cells, even when they are physically separated by a central lumen. This can be explained by secretion of paracrine growth factors, stimulating non-autonomous proliferation that is specific to Slik. We used genetic and transcriptomic assays to define the molecules and mechanism involved in Slik-mediated signaling. Contrary to what has been suggested, we found that Slik does not promote proliferation through the tumor suppressor Merlin (Mer, NF2 in mammals), an upstream component of the Hippo pathway, nor through other components of the Hippo pathway. Rather, Slik promotes non-autonomous proliferation and tissue growth signaling through dRaf (the single Raf family kinase orthologue in Drosophila). We found that dRaf is required in the signal receiving cells to stimulate proliferation. We performed RNA-seq to identify novel downstream effectors of Slik. Characterizing the signaling pathway downstream of Slik in Drosophila will shed light on how SLK and LOK function in mammals, and provide insights into their potential involvement during development and in cancer.